ArticleResearch and practice in thrombosis and haemostasis2020
Factor XIII deficiency does not prevent FeCl
Article in Research and practice in thrombosis and haemostasis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Review
- Fibrinogen and Factor XIII in Venous Thrombosis and Thrombus Stability.Arteriosclerosis, thrombosis, and vascular biology · 2022Review
- Role of Neutrophils and NETs in Animal Models of Thrombosis.International journal of molecular sciences · 2022Review
- Novel venous thromboembolism mouse model to evaluate the role of complete and partial factor XIII deficiency in pulmonary embolism risk.Journal of thrombosis and haemostasis : JTH · 2021Article
- The factor XIII-A Val34Leu polymorphism decreases whole blood clot mass at high fibrinogen concentrations.Journal of thrombosis and haemostasis : JTH · 2020Article
- Factor XIII deficiency does not prevent FeClResearch and practice in thrombosis and haemostasis · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe compositions of venous (red blood cell-rich) and arterial (platelet-rich) thrombi are mediated by distinct pathophysiologic processes; however, fibrin is a major structural component of both. The transglutaminase factor XIII (FXIII) stabilizes fibrin against mechanical and biochemical disruption and promotes red blood cell retention in contracted venous thrombi. Previous studies have shown factor XIII (FXIII) inhibition decreases whole blood clot mass and therefore, may be a therapeutic target for reducing venous thrombosis. The role of FXIII in arterial thrombogenesis is less studied, and the particular contribution of platelet FXIII remains unresolved.
objectiveTo determine whether FXIII reduction prevents experimental arterial thrombogenesis.
methodsUsing wild-type mice and mice with genetically imposed deficiency in FXIII, we measured thrombus formation and stability following ferric chloride-induced arterial thrombosis. We also determined the impact of FXIII on the mass of contracted platelet-rich plasma clots.
resultsFollowing vessel injury,
conclusionsFXIII does not significantly alter the underlying pathophysiology of experimental arterial thrombus formation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.